AcutePancreatitisIntroductionPancreatitis is an uncommon disease char - PDF document

AcutePancreatitis:IntroductionPancreatitis is an uncommon disease characterized by inflammation of the pancreasAcute pancreatitis affects about 50,00080,000 Americans each year. It is a condition that arises suddenly and may be quite severe, although patients usually have a completrecovery from an acuteattack.The pancreas is located deep in the retroperitoneal FigureA,Acuteinterstitialpancreatitis;B,acutehemorrhagicpancreatitis. FigureLocationthe pancreasthebody. AcutePancreatitis:AnatomyAnatomyThe pancreas lies behind the peritoneum of the posterior abdominal wall and is oblique in its orientation. The head of the pancreas is on the right side and lies within the “C” curve of the duodenum at the second vertebral level (L2). The tip of the pancreas extends across the abdominal cavity almost to the spleen. Collecting ducts empty digestive juices into the pancreatic duct, which runs from the head to the tail of the organ. The pancreatic duct empties into the duodenum at the duodenal papilla, alongside the common bile duct (Figure3).The Duct of Wirsung is the main pancreatic duct extending from the tail of the organ to the major duodenal papilla or Ampullaof Vater . The widest part of the duct is in the head of the pancreas (4 mm), tapering to 2mm at the tail in adults. The duct of Wirsung is close, and almost parallel, to the distal common bile duct before combining to form a common duct channel prior to approaching the duodenum. In approximately 70% of people, an accessory pancreatic duct of Santorini (dorsal pancreatic duct) is present. This duct may communicate with t

he main pancreatic duct. The degree of communication of the dorsal and ventral duct varies from patient to patient (Figure4).Smooth circular muscle surrounding the end of the common bile duct (biliary sphincter) and main pancreatic duct (pancreatic sphincter) fuses at the level of the ampulla of Vater and is called the sphincter of Oddi (Figure 4).This musculature is embryologically, anatomically, and physiologically different from the surrounding smooth musculature of the duodenum. The normal appearance through the endoscope includes the major and minor papilla. The major papilla extends 1cm into the duodenum with an orifice diameter of 1 mm. The minor papilla is 30 mm proximal and medial. Its orifice is tiny and may be difficult to identify (Figure 4B). Dysfunction of this muscle may result in unexplained abdominal pain or pancreatitis FigureAnatomymajorminorpapilla;grossappearance;B,sphincterOddimuscles;C, endoscopicview. FigureThepancreasadjacentanatomy. The sphincter of Oddi is a dynamic structure that relaxes and contracts to change the dimensions of the ampulla of Vater.The pancreas may be divided into five major regionsthe head, neck, body, tail and uncinate process (Figure 6). The distal end of the common bile duct can be found behind the upper border of the head of the pancreas. This duct courses the posterior aspect of the pancreatic head before passing through the head to reach he ampulla of Vater (major papilla). The uncinate process is the segment of pancreatic tissue that extends from the posterior of the head. The neck of the pancreas, a part of the gland

34 cm wide, joins the head and body. The pancreatic body lies against the aorta and posterior parietes, and anteriorly contacts the antrum of the stomach.CopyrightAllRightsReserved.NorthWolfeStreet,Baltimore,Maryland21287 FigureRegionsthepancreas. FigureFunctionthesphincterOddi;A,relaxed;B,contracted. AcutePancreatitis:CausesGallstonesGallstones are the most common cause of pancreatitis in the United States and other Western countries. Biliary tract disease accounts for 3550% of all cases. Despite aggressive and intensive early management, the mortality rate is approximately 10%. Although the exact mechanism of acute pancreatitis due to gallstones is not completely understood, most investigators believe that obstruction of the major papilla by the stone causes reflux of bile into the pancreatic duct (Figure 7). The presence of bile inthe pancreatic duct appears to initiate a complex cascade effect that results in acute pancreatitis.AlcoholAlcohol is the second leading cause of acute pancreatitis in Western countries. In many patients, however, chronic pancreatitis is already established. Alcohol is believed to cause acute pancreatitis by severalmechanisms. These include abnormal sphincter of Oddi motility, direct toxic and metabolic effects, and small duct obstruction by protein plug formation (Figure8).DrugsDrugs are a wellrecognized cause of pancreatitis. These drugs may be divided into those that have a definite association, and those with probable association with the development of acutepancreatitis. Table 01. FigureAlcoholinducedacutepancreatitis. FigureGallstoneobstru

ction. PancreasDivisumThe most common congenital anomaly of the pancreas, pancreas divisum, occurs in approximately 10% of the population, and results from incomplete or absent fusion of the dorsal and ventralducts during embryological development. In pancreas divisum, the ventral Duct of Wirsung empties into the duodenum through the major papilla but draining only a small portion of the pancreas (ventral portion). Other regions of the pancreas, including the tail, ody, neck and the remainder of the head, drain secretions into the duodenum through the minor papilla via the dorsal duct of Santorini (Figure 9).Recent clinical trials have supported the concept that obstruction of the minor papilla may cause acute pancreatitis or chronic pancreatitis in a subgroup of patients with pancreas divisum. Endoscopic or surgical therapy directed to the minor papilla has been effective in treating these patients. Figure 9 illustrates the appearance of pancreas divisum on endoscopic retrograde cholangiopancreatography (ERCP) in which most of the pancreas drains through the dorsal duct (hence the term dominant dorsal ductsyndrome).MicrolithiasisRecent studies have shown that a significant number of patients with idiopathic acute pancreatitis will have microlithiasis. This may be diagnosed either as gallbladder sludge on ultrasound (ultrasound of gallbladder sludge) or as crystals on microscopic examination of bile (Figure 10).Treatment of microlithiasis (by cholecystectomy, endoscopic sphincterotomy, or ursodeoxycholic acid) results in a significantreduction in the frequency of attacks of a

cutepancreatitis.MetabolicCausesHyperlipidemia and hypercalcemia may lead to acute pancreatitis. In patients with hyperlipidemia, triglyceride levels are usually greater than 2,000mg/dl. It is believed that lipase present in the pancreatic capillaries metabolizes the levels of triglyceride generating toxic free fatty acids. Hypercalcemia has been shown to induce experimental pancreatitis, probably by increasing pancreatic duct permeability. Its mechanism for the development of clinicalpancreatitis is not clear.Sphincter of OddiDysfunctionIn a small group of patients with recurrent pancreatitis of unknown etiology, manometric studies of the sphincter of Oddi have revealed abnormalities in motility. Clinical studies have shown that therapy, such as endoscopic or surgical sphincterotomy directed to the sphincter of Oddi, may be beneficial in these patients. Administration of nitrates or calcium channel blockers have provided shortterm relief in subsets of patients.Viral, bacterial, and parasitic infectious causes may lead to pancreatitis with mumps and Coxsackie B viruses being the most common. The human immunodeficiency virus (HIV) may cause elevation of serum pancreatic enzymes but rarely leads to severe pancreatitis. Bacterial infections that are associated with acute pancreatitiinclude Salmonella, Shigella, Campylobacter, Escherichia, Legionella, Leptospira, and even brucella. Pancreatitis associated with these infections is usually secondary to the release of toxins and usually is not the primary manifestation of such infections.MiscellaneousThere are multiple other causes of

acute pancreatitis that include scorpion stings, poisoning with organophosphorus insecticides, ascaris worms in the pancreatic duct, andtrauma.CopyrightAllRightsReserved.NorthWolfeStreet,Baltimore,Maryland21287 FigureMicrolithiasis;A,ultrasoundimagesludgemicrolithiasis;B,microscopicviewcrystals bile;grossappearance. FigurePancreasdivisum. AcutePancreatitis:DiagnosisDiagnosticCriteriaTableTableTableLaboratoryTestingIn acute pancreatitis, enzymes are released into the blood. Measurements of these enzymes are useful in the diagnosis of acute pancreatitis. The most common enzymes measured are amylase and lipase. Elevations of amylase are more sensitive, but less specific than lipase in the diagnosis of acute pancreatitis. Creactive protein, immunolipase, trypsinogen, and immunoelastase are all elevated following an acute attack of acute pancreatitis. Elevation of alanine aminotransferase and aspartate aminotransferase is predictive of gallstonepancreatitis.RadiologicalTestingAbdominal radiographs and standard chest films should routinely be performed on patients with severe abdominal pain. Patientswith pancreatitis may have a variety of radiological findings, such as pleural effusion, intestinal gas patterns, colonic obstruction, loss of psoas margins, and increased separation between the stomach and colon, suggesting inflammation of the pancreas. Calcification in the pancreas or calcified gallstones may also be noted.Ultrasound and computed tomography (CT) scans may be used to diagnose acute pancreatitis. Ultrasonography is not a sensitive test because overlying intestinal gas a

nd fatty tissue may obscure the pancreas in over one third of patients. However, ultrasound is very sensitive for the detection of gallstones, bile duct stones, and bile duct dilatationCT is the best diagnostic test for the diagnosis of acute pancreatitis. Contrastenhanced CT is excellent for diagnosis of pancreatic necrosis. Dynamic CT (performedby rapid injection of large doses of intravenous contrast) is highly predictive of pancreatic necrosis (Figure 11). EndoscopicDiagnosisGastrointestinal endoscopy allows the physician to visualize and biopsy the mucosaof the upper gastrointestinal tract. Endoscopy permits visualization of the esophagus, stomach and duodenum. During these procedures, the patient may be given a pharyngeal topical anesthetic that helps to prevent gagging. Pain medication and a sedative may also be administered before the procedure. The patient is placed in the left lateral position (Figure12).An endoscope, a thin, flexible, lighted tube, is passed through the mouth and pharynx and into the esophagus. The endoscope transmits an image of the esophagus, stomach, and duodenum to a monitor, which is visible to the physician. The endoscope is in position for the performance of endoscopic retrograde cholangiopancreatography (ERCP) when the tip is situated in the region of the major papilla (Figure 13).The endoscopy room is also equipped with an xray machine and monitor screen, which are used to help the physician visualize bile and pancreatic ducts. The endoscope also introduces air into the stomach, expanding the folds of tissue and enhancing the examination of the

stomach.Endoscopic Retrograde Cholangiopancreatography (ERCP) FigurePlacementendoscopeforERCP FigureRoomsetpatientpositioningforendoscopy. Figurescansshowing:mild;B,moderate;severepancreatitis. ERCP is an endoscopic technique for visualization of the bile and pancreatic ducts. During this procedure, the physician inserts a sideviewing endoscope (Figure 14) in the duodenum facing the major papilla (Figure 15). The sideviewing endoscope (duodenoscope) is specially designed to facilitate placement of endoscopic accessories into the bile and pancreatic duct. The endoscopic accessories may be passed through the biopsy channel (Figure 14) into the bile and pancreatic ducts. A catheter is used to inject dye into both pancreatic and biliary ducts to obtain xray images using fluoroscopy (Figure 15). During this procedure, the physician is able to see two sets of images: the endoscopic image of the duodenum andmajor papilla, and the fluoroscopic image of the bile and pancreatic ducts.The scope is designed to be held in the left hand with the thumb operating up and down angulation. The index finger operates the suction and air/water operations. The right hand is responsible for advancing, withdrawing and torquing the insertion tube. The right hand also operates left and right angulation of the endoscope, and passes accessories through theinstrument.A variety of instruments can be utilized through the endoscope (Figure 14). Electrosurgical devices such as snares, biopsy forceps, heater probes, BICAP devices for polyp removal and cauterization, dilation balloons, stents, catheters, an

d esophageal prostheses can also be used. Lithotripsy devices, injection devices, brushes, forceps, scissors, and magnetic extraction devices may also be inserted through the endoscope. Cameras may be attached for photo documentation and dual examiner viewing. Video cameras may also be attached for fullcolor motion picture viewing during endoscopic procedures or for later review.ERCP is a sensitive and specific diagnostic tool in acute pancreatitis. ERCP shows details of the pancreatic ductal anatomy including strictures, rupture, and pseudocysts (Figure15).ERCP and Sphincter of OddiManometryManometry of the sphincter of Oddi requires a sophisticated system to record the motility pattern of the sphincter of Oddi. Measurements are obtained using a special system of manometry catheters, a hydraulic capillary infusion system, and a computer software program. The fluid infusion system is of low compliance, allowing direct measurements of the sphincter of Oddi pressure. The standard manometry catheters are triple lumen and made of polyethylene or Teflon. Each catheter lumen has an internal diameter of 0.5 mm with three side holes at 2mm intervals starting at 10 mm from the tip. The catheters, which are 200 cm long, have an outer diameter of 1.7 mm. The pneumatic capillary system perfuses deionized, bubblefree water at a pressure of 750 mm Hg at a rate of 0.125 ml/min. Basal sphincter pressure, amplitude, and frequency of contractions as well as sequences of sphincter contractions may be obtained (Figure 16). Sphincter of Oddi dysfunction is diagnosed when the basal sphincter pressu

re is greaterthan 40 mm Hg. FigureA,NormalbiliarypancreaticductsduringERCP;ERCPimage. FigureSideviewingendoscope Copyright 2001All Rights Reserved. 600 North Wolfe Street, Baltimore, Maryland21287 FigureSphincterOddimanometry;setup;B,B’,endoscopicimagepositionof manometrycatheter. AcutePancreatitis:TherapyOverviewThe most important aspect in the treatment of acute pancreatitis is supportive care. This includes replacement of fluid and electrolytes, correction of metabolic abnormalities such as symptomatic hypercalcemia, and nutritional support. Other measures such as the use of nasogastric suction and antibiotics should be decidon a casecasebasis.MedicalTherapyAgents that have been used to inhibit pancreatic secretion, including somatostatin and glucagon, have not been found to be useful in altering the course in acute pancreatitisProtease inhibitors, which are effective in laboratory studies, have not been shown to be useful in clinical pancreatitisSurgicalTherapyEmergency surgery is not indicated in mild acute pancreatitis. Some surgical procedures such as resection of necrotic tissue and peritoneal lavage may have a role in select patients with severe, progressive necrotizing pancreatitis or pancreatic abscessCholecystectomy has been demonstrated to be effective in patients with recurrent acute pancreatitis and crolithiasis (Figure17).Surgical sphincteroplasty of the pancreatic sphincter is an alternative approach to endoscopic pancreatic sphincterotomy in patients with pancreatic sphincter dysfunction. Although the patient outcome is the same as for the endoscopic approac

h, it is more invasive, requiring laparotomy and duodenotomy Sphincteroplasty of the minor papilla is indicated for unsuccessful or failed endoscopic minor papilla sphincterotomy in patients with pancreas divisum EndoscopicTherapyEndoscopic therapy has a therapeutic role in three specific areas in the management of acute pancreatitis: 1) acute gallstone pancreatitis, 2) recurrent pancreatitis due to pancreatic sphincter dysfunction, and 3) recurrent pancreatitis due to pancreas divisum. The rationale for endoscopic therapy in each area is the relief of obstruction to the flow of pancreaticjuice.Acute GallstonePancreatitisAlthough it wouldseem logical that removal of the gallstones from the common bile duct early in acute gallstone pancreatitis would improve the clinical course, there is a lack of a “predictable” good outcome as suggested by prospective clinical trials. It appears, however, that the patients with suspected stones who benefit from early ERCP are those with evidence of biliary obstruction such as jaundice or dilation of the bile duct and severe pancreatitis. Further clinical trials are needed before more definitive recommendations can be made. In a subgroup of patients with acute recurrent pancreatitis and microlithiasis, endoscopic sphincterotomy has been shown to significantly reduce the frequency of attacks (Figure18). FigureA,B,TechniquecholecystectomywithA’,B’,laparoscopicview. Figure 18. AC, Endoscopicbiliarysphincterotomy with stone removal;A',B',endoscopic views and ERCP images. Recurrent Pancreatitis and Pancreatic SphincterDysf

unction ith the advent of manometric studies of the pancreatic sphincter, many cases of socalled idiopathic recurrent pancreatitis are now known to be a result of pancreatic sphincter dysfunction. Endoscopic pancreatic sphincterotomy may be expected to have a good outcome in up to 90% of these patients (Figure 19). Figure 19.Endoscopic majorpapillasphincterotomyandstent placement, AD', endoscopic views. PancreasDivisumEndoscopic minor papilla sphincterotomy is an effective treatment for patients with recurrent pancreatitis and pancreas divisum (Figure 20). Good longterm results are found in about 70% of patients but may be significantly less if there are changes of chronic pancreatitis Figure 20.C, Endoscopic minorpapillasphincterotomy performed with a pulltype sphincterotome; A’C’, endoscopic views. There are two techniques for endoscopic minor papilla sphincterotomy; one is with a pulltype sphincterotome followed by stenting of the pancreatic duct and the second is with a needleknife sphincterotome performed over a pancreatic stent (Figure 21). Following pancreatic sphincterotomy there may be tissue swelling that ould result in obstruction to pancreatic outflow. Therefore shortterm pancreatic stenting is indicated when pancreatic sphincterotomy is performed to maintain patency of pancreaticoutflow. Figure 21.A, B, Endoscopicsphincterotomyperformed with a needleknife sphincterotome over astent ; A’, B’, endoscopic views. OverviewComplications of acute pancreatitis may result in local or systemic problems. The systemic problems are usually seen

in acute, severe pancreatitis. These include pulmonary complications, such as pulmonary edema and adult respiratory distress syndrome. Inflammatory changes from the pancreas may extend to the kidneys, stomach, colon and splenic vein (Figure 22). This may result in renal dysfunction, gastrointestinal bleeding, colitis and splenic vein thrombosis. The management of these complications issupportive.Local complications include fluid collection, ascites , pancreatic pseudocyst, pancreatic necrosis, and infective pancreatic necrosis. These complications are twice as frequent in patients with alcoholic and biliarypancreatitis. FluidCollectionsFluid collections are common in patients with acute pancreatitis. Simple fluid collections resolve spontaneously in most patients, so therapy is not usually required. The presence of gas within a fluid collection suggests underlying infection and mandates therapy.PseudocystsThe most common complication of acute pancreatitis (occurring in approximately 25% of patients, especially those with alcoholic chronic pancreatitis) is the collection of pancreatic juices outside of the normal boundaries of the ductal system called pseudocysts (Figure 23A). Most pseudocysts resolve spontaneously. Mature pseudocysts are enclosed by membranes composed of fibrous tissue and are often situated in the body of the pancreas. They may be classified as communicating (connecting to the pancreatic duct) or noncommunicating (independent of the pancreatic duct) (Figure 23B).Although the mechanism of pseudocyst formation is speculative, it is thought to result from the rupt

ure of a pancreatic duct,activation of interstitial pancreatic juices, parenchymal necrosis, intraductal leakage, and local mesothelial cells reacting to walloff fluid collection by formation of a fibrous membrane.Pain is the major presenting symptom in cases of pancreatic pseudocysts. Transabdominal ultrasound is helpful in diagnosis and management of pseudocysts. CT scanning has also proved to be an accurate method of diagnosis and provides structural detail on duct size.Pseudocysts larger than 6 cm rarely spontaneously resolve. Although conservative management is recommended, intervention should be undertaken when symptoms of persistent abdominal pain, pseudocyst enlargement or complications occur. Treatment includes excision and internal or external drainage.EndoscopicTherapyDiagnostic endoscopic retrograde cholangiopancreatography (ERCP) is performed once the patient is considered an appropriate candidate for endoscopic drainage. Appropriate identification and management of ductal obstruction is important in management of pseudocysts.Transpapillary stent placement is recommended as an initial therapy for patients with relatively small pseudocysts that communicate with the main pancreatic duct. During this procedure, a biliary sphincterotomy is performed along with pancreatic sphincterotomy to avoid the potential for biliary obstruction. Dilation is carried out if ductal strictures are present. Obstructive pancreatic stones should also be removed. Pancreatic duct stents (usually 78.5 F, thinwalled) are placed in the pancreatic duct extending into the duodenum (Figure 24). The s

tent is removed with resolution of the pseudocyst, approximately 6 weeks later. The success rate is greater Figure23.Pancreaticpseudocystacutepancreatitis;B,communicatingcommunicating pseudocysts. Figure22.Organsinvolvedwithinflammatoryspread. than70%.Endoscopic Therapy for Noncommunicating PseudocystTransmural puncture is recommended for patients with large noncommunicating pseudocysts that compress the stomach or duodenumon CT scan. Especially in patients with complete obstruction of the duct, transmural puncture is the only feasible endoscopic alternative. All patients undergoing this procedure are given preoperativeantibiotics.A needleknife sphincterotome is used to create a small incision though the gastric or duodenal wall into the pseudocyst. After needleknife entry into the pseudocyst cavity, a guide wire is placed, followed by balloon dilation (Figure 25B). Finally, two or more catheter doublepigtailed stents are placed (Figure 25C), decompressing the pseudocyst (Figure 25D). Endoscopic ultrasound (EUS) or endoscopic needle localization may be used to guide the puncture and identify a safe entry site into the pseudocyst.SurgicalTherapySurgical management may be indicated for pancreatic pseudocysts with persistent symptoms, cyst enlargement or complications. Anastomosis of the internal pseudocyst to a portion of the gastrointestinal tract facilitates internal drainage. Usually the stomach, a RouxY limb of the proximal jejunum, or duodenum may be used. In cases where a pseudocyst is located in the body of the pancreas adherent to the stomach, a cystogastrostomy is performe

d (Figure 26A). Anterior gastrotomy is performed, the cyst is aspirated by needle, and a 3cm opening made. Anastomosis of the pseudocyst to the posterior gastric wall facilitates pseudocyst drainage (Figure26B).The RouxY cystojejunostomy is useful in draining multiple pseudocysts not adherent to the duodenum or the stomach. During this procedure, the pseudocyst is entered, its contents evacuated, and it is attached to the jejunal limbPseudocysts in the head of the pancreas are drained into the duodenum by transduodenal cystoduodenostomy. A site in the duodenum, in close proximity to the Figure26.Surgicalcystogastrostomyforpancreaticpseudocyst. Figure25.Endoscopictechniquefortransgastricpseudocystdrainage. Figure24.Transpapillarystentforcommunicatingpancreaticpseudocyst. pseudocyst, is identified and a lateral duodenotomy is made. The pseudocyst is entered through the medial wall of the duodenum. Sutures are placed to control bleeding and the lateral duodenotomy isclosed.PercutaneousTherapyAnother treatment option for pseudocyst management in chronic pancreatitis is percutaneous drainage (Figure 27, A and B).after.During percutaneous drainage, a needle is inserted through both gastric walls while the position of the catheter is monitoredwith a gastroscope or fluoroscope . Pseudocyst drainage into the stomach may be facilitated by placement of a doublepigtailed catheter. Alternately, an indwelling Jshaped catheter (Figure 28) facilitates external drainage and may be used in cases where pseudocyst contents are viscous. These methods are less invasivethan surgery and provide an al

ternative for patients who are at high risk for surgicalmanagement.PancreaticNecrosisPancreatic necrosis is a significant complication of acute pancreatitis, and may result in mortality rates as high as 15%. Whatever the mechanism of acute pancreatitis, in necrotizing pancreatitis, there is obstruction of the pancreatic microcirculation (Figure 29). This may be demonstrated by CT imaging, in which intravenously administered contrast materials will not appear in areas of necrosis. Dynamic contrastenhanced CT is the gold standard for the detection of pancreatic necrosis, with accuracy of greater than90%. Figure28.rayindwellingcatheterforpancreaticpseudocystdrainage. Figure27.Techniquepercutaneousdrainagepancreaticpseudocyst;A,before; InfectionPreventionLarger, controlled studies are needed to ascertain the effectiveness of prophylactic lavage and antibiotic therapy for the prevention of infection in patients with acute pancreatitis. Peritoneal lavage with 50 L/day and longterm lavage have been used in patients with severe necrosis to prevent infection. Ciprofloxacin, ofloxacin, imipenem, and metronidazole have been shown efficacious in infection prevention, although a combination of antibiotics may be most beneficial.InfectionDetectionAbdominal radiographs and CT scans are useful for the identification of areas of infection. CTguided needle aspiration of suspected infections should be examined cultured.Monomicrobial infection is uncommon but successfully treated, whereas the more frequent finding of polymicrobial infection is more resistant and leads to a poorer prognosis.Treatment

Treatment of infected pancreatic necrosis depends on the pattern and anatomic location. Surgical debridement of necrotic tissue or percutaneous drainage comprise the treatment options. Surgical debridement of infected tissue found early in the course of pancreatitis reduces mortality rates.PulmonaryInvolvementFluid accumulation within the pleural space with resultant lung compression, and respiratory distress syndrome are serious complications of pancreatitis. Acute pleural fluid collection, pancreaticpleural fistula , and effusions may result from acute inflammation of the pancreas. Most often, pleural effusions spontaneously resolve; however, thoracentesis is suggested in the face of respiratory compromise or infection. Respiratory support with peritoneal lavage has been shown to improve lung function in patients with severe adult respiratory distress syndrome.OtherComplicationsRenal dysfunction may accompany acute pancreatitis by direct extension of inflammation to the kidney. Erosion of vascular structures by abscesses or pseudocysts may cause gastrointestinal hemorrhage. Extension of pancreatic inflammation may also lead to colonic strictures, fistulas and perforation. Theinflammatory process may lead to splenic vein thrombosis or pseudocyst formation in the spleen (Figure 30).Splenectomy (Figure 31) is the preferred treatment for splenic vein thrombosis, pseudoaneurysm, or rupture. Figure30.Splenicveinthrombosiswithsplenomegaly. Figure29.Pancreaticnecrosis Copyright 2001All RightsReserved.NorthWolfeStreet,Baltimore,Maryland21287 Figure31.Splenectomy;preoperative;postoperative